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Effects of intravenously administered prostaglandin E1 on pain, vigilance and cognition in volunteers
Th. Hummel* and G. Kobal. Dept. of Pharmacology and Toxicology, University of Erlangen-Nuremberg,
Poster 99 ’ BROWN Mon-Tues ACC Hall E
West Gemtany
Abs No
EFFECTS OF INTRAVENOUSLY ADMINISTERED PROSTAGLANDIN E, ON PAIN, VIGILANCE AND COGNITION IN VOLUNTEERS
AIM OF INVESTIGATION: Prostagfandins exert a modifying effect on the sensitivity of nociceptors. The aim of the present study was to determine, whether
406
i
‘)
PGEl, administered perenterally, influences the
perception of experlmentalfy induced pain in humans, and, possibly, affects the central nervous system, too. METHODS: In 6 young, healthy volunteers (5 male, 1 female) the action of FGEt (60 jrg by infusion over 2 hours) was compared with placebo, using a controtfed, randomized, double-blind, P-fold cross-over design. Measurements were obtained before as well as 60 min and 120 min after administration of the drug. 16 C02-stimuli of painful intensities (duratfon 200 msec) were presented to the nasal mucosa, and 106 tone bursts (rare p=O.16, 2 kHz - frequent p=O.t34.t .5 kHz) were used as acoustic stimuli in order to record the cognitive component (P300). The EEG was recorded from 8 sites of the IO/26 classification. The following parameters were investigated: the quality and quantity of unwanted sideeffects. the pulse rate, the systolic and diastolic blood-pressure, the performing of a tracking task in a simple video game, the estimates of pain intensity, power spectra of the spontaneous EEG, and the amplitudes and latencies of the chemo-somatosensory
ano
acoustic evoked potentials (P306). RESULTS: In nearfy all of the subjects PGEI caused a venous irritation. There were no signfficant changes in the cardiovascular parameters, However, compared to placebo, the pulse rate showed a tendency lo rise after administration of PGEt. Neither pain related evoked potentials, nor the estfmates of pain intensity indicated a change in the perception of pain. There was no evidence of an increase or decrease of arousal in the power spectra, and the tracking performance was not influenced by PGEI, either. However. a signtflcant (t-test, ~~0.05) reduction in latency of the P300-component of the acoustic woked
potentials was observed, of which an improvement of the
cognitive capacity might be the explanation. CONCLUSION: PGEl dii not after the perception of experimentally induced pain, The possible improvement of cognitive capacity might be related to an Improved Mood circulation in the brain caused by PGEI
CEREBRAL POTENTIALS EVOKED BY ELECTRICAL NERVE AND CUTANEOUS/ HEAT STIMULI IN PATIENTS WITH DISSOCIATED SENSORY LOSS.
Poster 100 j BROWN Won-Tues
A. Frieling, J. Lankers, Institute of Physiology, 2000 Hamburg 52, FRG
Abs No
ACC
B. Bromm, University
of Hamburg,
Hall
E
407
A CO,-laser was used to elicit ultrashort (201~s) heat stimuli of 10.6pm wavelength that activate predominantly superficial A&- and C-fibres of hairy skin and cause a sensation of warmth and pain, depending on intensity. Laser stimuli evoke late cerebral potentials (LEP), that are delayed by appr. looms in comparison to late potentials after conventional electrical nerve stimulation (SEP), thus demonstrating the lower conduction velocity of the fibres involved. LEP are used to demonstrate clinical disorders of pain and temperature sensation. In 18 patients with dissociated sensory loss, LEP and SEP were tested, comparing an affected skin area with an undisturbed area. The clinical diagnoses, confirmed by CT and WRT imaging, were: syringomyelia (5), encephalomyelitis disseminata (4), myelitis (4), Brown Seguard Syndrome (2), Wallenberg Syndrome (l), spinal compression (l), cervical myelopathy (1). In 12 cases, LEP were found to be altered on the affected side: 6 were missing, 6 were significantly reduced. In contrast, in all cases SEP were normal. The 6 cases with normal LEP results in spite of dissociated sensory disturbances had an inflammatory etiology, whereas the 12 cases with altered LEP exhibited structural lesions of central pathways. Supported by the Deutsche Forschungsgemeinschaft (Br 310/16) We thank the Dept. of Neurology for referring the patients.
/ , I
Poster 99 ’ BROWN Mon-Tues ACC Hall E
West Gemtany
Abs No
EFFECTS OF INTRAVENOUSLY ADMINISTERED PROSTAGLANDIN E, ON PAIN, VIGILANCE AND COGNITION IN VOLUNTEERS
AIM OF INVESTIGATION: Prostagfandins exert a modifying effect on the sensitivity of nociceptors. The aim of the present study was to determine, whether
406
i
‘)
PGEl, administered perenterally, influences the
perception of experlmentalfy induced pain in humans, and, possibly, affects the central nervous system, too. METHODS: In 6 young, healthy volunteers (5 male, 1 female) the action of FGEt (60 jrg by infusion over 2 hours) was compared with placebo, using a controtfed, randomized, double-blind, P-fold cross-over design. Measurements were obtained before as well as 60 min and 120 min after administration of the drug. 16 C02-stimuli of painful intensities (duratfon 200 msec) were presented to the nasal mucosa, and 106 tone bursts (rare p=O.16, 2 kHz - frequent p=O.t34.t .5 kHz) were used as acoustic stimuli in order to record the cognitive component (P300). The EEG was recorded from 8 sites of the IO/26 classification. The following parameters were investigated: the quality and quantity of unwanted sideeffects. the pulse rate, the systolic and diastolic blood-pressure, the performing of a tracking task in a simple video game, the estimates of pain intensity, power spectra of the spontaneous EEG, and the amplitudes and latencies of the chemo-somatosensory
ano
acoustic evoked potentials (P306). RESULTS: In nearfy all of the subjects PGEI caused a venous irritation. There were no signfficant changes in the cardiovascular parameters, However, compared to placebo, the pulse rate showed a tendency lo rise after administration of PGEt. Neither pain related evoked potentials, nor the estfmates of pain intensity indicated a change in the perception of pain. There was no evidence of an increase or decrease of arousal in the power spectra, and the tracking performance was not influenced by PGEI, either. However. a signtflcant (t-test, ~~0.05) reduction in latency of the P300-component of the acoustic woked
potentials was observed, of which an improvement of the
cognitive capacity might be the explanation. CONCLUSION: PGEl dii not after the perception of experimentally induced pain, The possible improvement of cognitive capacity might be related to an Improved Mood circulation in the brain caused by PGEI
CEREBRAL POTENTIALS EVOKED BY ELECTRICAL NERVE AND CUTANEOUS/ HEAT STIMULI IN PATIENTS WITH DISSOCIATED SENSORY LOSS.
Poster 100 j BROWN Won-Tues
A. Frieling, J. Lankers, Institute of Physiology, 2000 Hamburg 52, FRG
Abs No
ACC
B. Bromm, University
of Hamburg,
Hall
E
407
A CO,-laser was used to elicit ultrashort (201~s) heat stimuli of 10.6pm wavelength that activate predominantly superficial A&- and C-fibres of hairy skin and cause a sensation of warmth and pain, depending on intensity. Laser stimuli evoke late cerebral potentials (LEP), that are delayed by appr. looms in comparison to late potentials after conventional electrical nerve stimulation (SEP), thus demonstrating the lower conduction velocity of the fibres involved. LEP are used to demonstrate clinical disorders of pain and temperature sensation. In 18 patients with dissociated sensory loss, LEP and SEP were tested, comparing an affected skin area with an undisturbed area. The clinical diagnoses, confirmed by CT and WRT imaging, were: syringomyelia (5), encephalomyelitis disseminata (4), myelitis (4), Brown Seguard Syndrome (2), Wallenberg Syndrome (l), spinal compression (l), cervical myelopathy (1). In 12 cases, LEP were found to be altered on the affected side: 6 were missing, 6 were significantly reduced. In contrast, in all cases SEP were normal. The 6 cases with normal LEP results in spite of dissociated sensory disturbances had an inflammatory etiology, whereas the 12 cases with altered LEP exhibited structural lesions of central pathways. Supported by the Deutsche Forschungsgemeinschaft (Br 310/16) We thank the Dept. of Neurology for referring the patients.
/ , I